Mycotoxins are toxic substances produced by molds, which cause disease in animals or man. Acute diseases caused by mycotoxins are called mycotoxicoses. History has recorded several human disease outbreaks and numerous animal poisonings thought to be mycotoxicoses. The outbreak of Turkey X disease in England in 1960 culminated in the discovery of aflatoxins and the realization that low levels of mold metabolites in foods and feed could cause disease in man and animals. This gave great impetus to the study of mycotoxins. Mycotoxin-producing molds are quite ubiquitous and frequently contaminate food and agricultural commodities. Fortunately, the mere presence of a toxic mold in food does not automatically mean the presence of mycotoxins. Mycotoxins currently receiving the most attention as potential hazards to human and animal health include aflatoxins, ochratoxin A, sterigmatocystin, patulin, penicillic acid, citrinin, zearalenone and the toxic trichothecenes. These compounds all cause some degree of acute toxicity when given in high amounts. In addition, aflatoxins, sterigmatocystin, patulin and penicillic acid are potential carcinogens.

The significance of mycotoxins as causes of human diseases is difficult to determine because there is no direct evidence of such involvement in terms of controlled experiments with man. Human cases of ergotism and alimentary toxic aleukia are known to be of fungal origin. Recent reports have linked aflatoxins to acute poisonings of humans in Africa, southeast Asia and India. Epidemiological studies have correlated aflatoxin contamination of foodstuffs with high incidences of liver cancer and other liver disease in certain regions of the world. It has been suggested that ochratoxin A may be involved in a fatal kidney disease of humans known as Balkan Endemic Nephropathy. Ochratoxin A has been found in foodstuffs from the endemic areas of this disease.

Mycotoxins may enter the food supply by direct contamination, resulting from mold growth on the food, or by indirect contamination through the use of contaminated ingredients in processed foods. Indirect exposure to mycotoxins can also result from consumption of animal products, such as milk, which contain mycotoxin residues. caused by feeding moldy feed to the food-producing animal. Commodities susceptible to direct contamination with mycotoxins include nuts, oilseeds, grains and to a limited extent, certain fruits. Residues of aflatoxin have been found in animal products such as fluid milk, nonfat dry milk, cottage cheese and imported cheeses. In feeding experiments with aflatoxins, the toxins were found in livers, kidneys and certain tissues of pigs and broiler chickens, and in eggs from laying hens fed aflatoxin. Residues of ochratoxin A have been found in livers, kidneys, muscle and adipose tissues of bacon pigs and poultry. Refrigerated foods, such as cheeses, cured meats and certain flour-based products, subject to mold growth during storage, have been shown to be contaminated with a variety of potential mycotoxin-producing molds. Experimental evidence indicates that certain mycotoxins could be produced on refrigerated foods under certain conditions. Aflatoxin production is favored by temperatures of 20 to 25 C; but has been reported to occur as low as 7 to 12 C. Toxins produced by Penicillium species can be produced at temperatures as low as 5 C; however, patulin and penicillic acid do not appear to be produced to any extent on substrates such as cheeses and cured meats. Aflatoxins and ochratoxins appear to be relatively stable in most foods, whereas patulin and penicillic acid are not stable in proteinaceous foods such as cheeses and meats. Stability data on other mycotoxins are lacking for most foods. In general, mycotoxins are most stable in grains, nuts and oilseeds. The current tolerance level for aflatoxins in foods is 20 ppb, which will probably be lowered to 15 ppb in the near future. Recently, an action level of 0.5 ppb for aflatoxin in milk and milk products was announced which is essentially a tolerance level for these products.

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Author notes

1Published as Paper No. 5548, Journal Series, Nebraska Agricultural Experiment Station, Project 16-022. This research was supported by the University of Nebraska-Lincoln Research Council and NIH Biomedical Research Support Grant RR-07055.

2Presented in part at the 63rd Annual Meeting of the International Association of Milk, Food and Environmental Sanitarians, Arlington Heights, Illinois, August 8–11, 1976.